Rhonda Patrick· PhD
Vitamin D deficiency (affecting serotonin synthesis)
The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
Vitamin D deficiency (affecting serotonin synthesis)
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I published a couple of papers a few years ago first identifying how vitamin D regulates the conversion of tryptophan into serotonin (which plays a key role in the brain development) and how this may relate to the development of autism, ADHD, and more.
if a mom is deficient in vitamin D doesn't have enough vitamin D there may not be enough vitamin D getting into the fetal brain to activate tph to to convert tryptophan into serotonin as a consequence this could lead to abnormal brain development
another group independently confirmed biochemically that vitamin D hormone indeed does activate tryptophan hydroxy to in various different neuronal cell populations so it does increase the expression of the gene this has been validated biochemically
and possibly lead to autistic like behaviors so how does this occur well I mentioned that in addition to vitamin D turning on the gene that makes serotonin in the brain it turns off the gene that makes serotonin in the gut also in the placenta so tryptophan not only gets metabolized into serotonin by tryptophan hydroxylase but there's another pathway an enzyme called Ido which also converts tryptophan into something called curine which then gets converted into t-regulatory cells t-regulatory cells are very important immune cells that are essential to prevent your body from having an autoimmune response to prevent your your body's immune cells from attacking its own tissue in mice it's been shown that that if you delete the enzyme Ido so that tryptophan cannot be metabolized into curine or into the t- regulatory cells female mice have such a when they're pregnant they have such a strong autoimmune response against the fetus that their immune system actually kills the fetus and it's obviously a very severe condition but that's been shown to be dependent on the fact that these mice cannot make curin and anti-regulatory cells so tryptophan actually binds much more tightly to tryptophan Hydrox one compared to Ido so we think under conditions of low vitamin D the tph1 is not being turned off it's not being regulated normally and this leads to aarant expression of this enzyme you're making too much of it which then acts as a tryptophan trap a sink for tryptophan so now tryptophan's only getting metabolized into serotonin and it's not going to be producing enough of the T regulatory cells um potentially when this is happening during pregnancy this could lead to maybe a uh a little bit of an autoimmune response and possibly cause you know the the mother's immune cells to then start making antibodies against fetal brain tissue